<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-18T23:54:18Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10128" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10128</identifier><datestamp>2026-10-18T21:13:07Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Protective effects of multi-strain probiotics against polystyrene nanoplastic-induced parotid gland toxicity: role of NRF2/HO-1 and NF-κB pathways</dc:title><dc:creator>Kozan, Günay</dc:creator><dc:creator>Üstündağ, Hilal</dc:creator><dc:creator>Kara, Adem</dc:creator><dc:subject>inflammation</dc:subject><dc:subject>nanoplastics</dc:subject><dc:subject>Nrf2 pathway</dc:subject><dc:subject>oxidative stress</dc:subject><dc:subject>parotid gland</dc:subject><dc:subject>polystyrene</dc:subject><dc:subject>probiotics</dc:subject><dc:subject>aquaporin 5</dc:subject><dc:subject>heme oxygenase 1</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>ketamine</dc:subject><dc:subject>nanoplastic</dc:subject><dc:subject>probiotic agent</dc:subject><dc:subject>protein bcl 2</dc:subject><dc:subject>transcription factor Nrf2</dc:subject><dc:subject>xylazine</dc:subject><dc:subject>acinar cell</dc:subject><dc:subject>adult</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>antioxidant activity</dc:subject><dc:subject>Article</dc:subject><dc:subject>bacterial strain</dc:subject><dc:subject>Bifidobacterium</dc:subject><dc:subject>Bifidobacterium longum</dc:subject><dc:subject>controlled study</dc:subject><dc:subject>disease severity</dc:subject><dc:subject>down regulation</dc:subject><dc:subject>histopathology</dc:subject><dc:description>Background – Polystyrene nanoplastics (NPs) represent emerging environmental contaminants with potential adverse effects on salivary glands. This study investigated the protective effects of multi-strain probiotics against NPs-induced toxicity in rat parotid glands. Methods – Forty male Sprague-Dawley rats were allocated into five groups (n = 8): control, NPs (10 mg/kg), probiotics (1010 CFU), NPs + probiotics low dose (109 CFU), and NPs + Pro high dose (1010 CFU). Treatments were administered orally for 35 days. Oxidative stress markers, histopathological changes, and protein expression were evaluated. Results – NPs exposure significantly increased MDA levels (p &lt; 0.05) and decreased SOD activity and GSH content (p &lt; 0.05). Histopathological examination revealed moderate to severe acinar degeneration (++) and fibrosis (++) in NPs-treated animals. Western blot analysis showed significant downregulation of Bcl-2 (p &lt; 0.01), HO-1 (p &lt; 0.0001), NRF2 (p &lt; 0.01), and AQP5 (p &lt; 0.0001), with upregulation of Caspase-3 (p &lt; 0.0001), NF-κB (p &lt; 0.001), IL-1β (p &lt; 0.001), and TNF-α (p &lt; 0.001). Probiotic supplementation significantly ameliorated oxidative stress (p &lt; 0.05), reduced histopathological damage to mild changes (+), and restored beneficial protein expression while suppressing inflammatory markers (p &lt; 0.01-0.001). Conclusion – This study provides the first evidence that NPs induce significant oxidative stress and tissue damage in parotid glands. Multi-strain probiotics provide substantial protection by activating the NRF2/HO-1 pathway and suppressing inflammation, suggesting a promising therapeutic strategy against nanoplastic-induced oral tissue damage. Copyright © 2026 Kozan, Üstündağ and Kara.</dc:description><dc:publisher>Frontiers Media SA</dc:publisher><dc:date>2026</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/10128</dc:identifier><dc:identifier>https://doi.org/10.3389/fphar.2026.1824052</dc:identifier><dc:identifier>1663-9812</dc:identifier><dc:language>en</dc:language><dc:relation>Frontiers in Pharmacology</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/10128</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>